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PMID: 16243356 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Trim32 is a ubiquitin ligase mutated in limb girdle muscular dystrophy type 2H that binds to skeletal muscle myosin and ubiquitinates actin.

Journal of molecular biology ·Vol. 354 ·No. 2 ·2005-11-25 ·Pages 413-24

Kudryashova E, Kudryashov D, Kramerova I, Spencer MJ

Abstract

Trim32 belongs to the tripartite motif (TRIM) protein family, which is characterized by a common domain structure composed of a RING-finger, a B-box, and a coiled-coil motif. In addition to these motifs, Trim32 possesses six C-terminal NHL-domains. A point mutation in one NHL domain (D487N) has been linked to two forms of muscular dystrophy called limb girdle muscular dystrophy type 2H and sarcotubular myopathy. In the present study we demonstrate that Trim32 is an E3 ubiquitin ligase that acts in conjunction with ubiquitin-conjugating enzymes UbcH5a, UbcH5c, and UbcH6. Western blot analysis showed that Trim32 is expressed primarily in skeletal muscle, and revealed its differential expression from one muscle to another. The level of Trim32 expression was elevated significantly in muscle undergoing remodeling due to changes in weight bearing. Furthermore, expression of Trim32 was induced in myogenic differentiation. Thus, variability in Trim32 expression in different skeletal muscles could be due to induction of Trim32 expression upon changes in physiological conditions. We show that Trim32 associates with skeletal muscle thick filaments, interacting directly with the head and neck region of myosin. Our data indicate that myosin is not a substrate of Trim32; however, Trim32 was found to ubiquitinate actin in vitro and to cause a decrease in the level of endogenous actin when transfected into HEK293 cells. In conclusion, our results demonstrate that Trim32 is a ubiquitin ligase that is expressed in skeletal muscle, can be induced upon muscle unloading and reloading, associates with myofibrils and is able to ubiquitinate actin, suggesting its likely participation in myofibrillar protein turnover, especially during muscle adaptation.

MeSH Terms
Actins/metabolism Animals Blotting, Western Cell Differentiation Cells, Cultured Hindlimb Suspension Kidney/metabolism Male Mice Muscle Proteins/genetics,immunology,metabolism Muscle, Skeletal/metabolism Muscular Dystrophies, Limb-Girdle Mutation/genetics Myofibrils/metabolism Peptide Fragments/immunology Protein Binding Rabbits Saccharomyces cerevisiae/genetics,growth & development,metabolism Skeletal Muscle Myosins/metabolism Subcellular Fractions Two-Hybrid System Techniques Ubiquitin/metabolism Ubiquitin-Conjugating Enzymes/metabolism Ubiquitin-Protein Ligases/genetics,immunology,metabolism
Chemicals
Actins Muscle Proteins Peptide Fragments Ubiquitin Ubiquitin-Conjugating Enzymes Ubiquitin-Protein Ligases Skeletal Muscle Myosins
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Kudryashova Elena
Department of Neurology and Pediatrics, Duchenne Muscular Dystrophy Research Center, University of California at Los Angeles, CA 90095, USA.
Kudryashov Dmitri
Kramerova Irina
Spencer Melissa J
Article Info
Journal
Journal of molecular biology
Abbr.
J Mol Biol
ISSN
0022-2836
Published
2005-11-25
Epub
2005-00-10
Pages
413-24
Language
English
Region
England
NLM ID
2985088R
Subset
IM
Grants
NIAMS NIH HHS · AR48177 · United States
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